The food pyramid recommended 6-11 servings of carbs per day, and very little fat — a low-fat, high-carb diet. As we outlined in our last video, type 2 diabetes is a disease of carbohydrate intolerance. Someone with type 2 diabetes or prediabetes has a low carbohydrate tolerance, so eating carbs will lead to exaggerated blood sugar spikes. While those with a high carb tolerance may be able to eat a carb-heavy diet and remain healthy, someone with a low carb tolerance will experience chronic high blood sugar and likely even weight gain if they eat a high-carb diet.
By checking your own blood sugar levels, you can track your body's changing needs for insulin and work with your doctor to figure out the best insulin dosage. People with diabetes check their blood sugar up to several times a day with an instrument called a glucometer. The glucometer measures glucose levels in a sample of your blood dabbed on a strip of treated paper. Also, there are now devices, called continuous glucose monitoring systems (CGMS), that can be attached to your body to measure your blood sugars every few minutes for up to a week at a time. But these machines check glucose levels from skin rather than blood, and they are less accurate than a traditional glucometer.
It was once assumed that environmental factors took generations to affect a gene change, but research is now finding that a bad enough toxin or environmental stress can alter genes in a single generation. While genes can pre-dispose us to disease, the disease will only present itself in the presence of factors like toxins, poor diet or stress. A predisposition to diabetes, for instance, might be activated from toxins in foods, pesticides, herbicides, chemicals, or from a poor diet, especially when any of the above factors are also present.
Other medications such as metformin or the DPP4 drug class are weight neutral. While this won’t make things worse, they won’t make things better either. Since weight loss is the key to reversing type 2 diabetes, medications won’t make things better. Medications make blood sugars better, but not the diabetes. We can pretend the disease is better, but that doesn’t make it true.
Exenatide (Byetta) was the first drug of the GLP-1 agonist group. It originated from an interesting source, the saliva of the Gila monster. Scientists observed that this small lizard could go a long time without eating. They discovered a substance in its saliva that slowed stomach emptying, thus making the lizard feel fuller for a longer time. This substance resembled the hormone GLP-1.

Cloves protect the heart, liver and lens of the eye of diabetic rats, according to studies. This spice contains 30% of the antioxidant phenol in dry weight, along with antioxidants anthocyanins and quercetin. As a result, cloves have antiseptic as well as germicidal properties. It also offers anti-inflammatory, analgesic and digestive health benefits for diabetics.

Physical activity is an important part of controlling diabetes and preventing complications such as heart disease and high blood pressure. "We know that exercise is a very effective way to help bring blood sugars under control for someone with type 2 diabetes," says Kenneth Snow, M.D., Acting Chief, Adult Diabetes, Joslin Clinic. Try for 30 minutes of moderate exercise, like brisk walking, on most days. Joslin's Why WAIT? and Easy Start exercise programs are great resources for developing a safe weight loss program.
Recent research shows that the first step in Diabetes management should be for patients to be put on a low carb diet. Patients that are put on a high carb diet find it very difficult to maintain normal blood glucose levels. Patients that are put on a low carb or restricted carbohydrate diet, manage to maintain near normal blood glucose levels and A1cs.[29][30][31][32][33][34][35][36][37]
The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
This section deals only with approaches for curing the underlying condition of diabetes type 1, by enabling the body to endogenously, in vivo, produce insulin in response to the level of blood glucose. It does not cover other approaches, such as, for instance, closed-loop integrated glucometer/insulin pump products, which could potentially increase the quality-of-life for some who have diabetes type 1, and may by some be termed "artificial pancreas".
Eating right and exercising more often is good for everyone. But it's especially important for people with type 2 diabetes. When people put on too much body fat, it's because they're eating more calories than they use each day. The body stores that extra energy in fat cells. Over time, gaining pounds of extra fat can lead to obesity and diseases related to obesity, like type 2 diabetes.
Diabetic persons must increase their awareness about oral infections as they have a double impact on health. Firstly, people with diabetes are more likely to develop periodontal disease, which causes increased blood sugar levels, often leading to diabetes complications. Severe periodontal disease can increase blood sugar, contributing to increased periods of time when the body functions with a high blood sugar. This puts diabetics at increased risk for diabetic complications.[58]
The earliest predictor of the development of type 2 diabetes is low insulin sensitivity in skeletal muscle, but it is important to recognize that this is not a distinct abnormality but rather part of the wide range expressed in the population. Those people in whom diabetes will develop simply have insulin sensitivity, mainly in the lowest population quartile (29). In prediabetic individuals, raised plasma insulin levels compensate and allow normal plasma glucose control. However, because the process of de novo lipogenesis is stimulated by higher insulin levels (38), the scene is set for hepatic fat accumulation. Excess fat deposition in the liver is present before the onset of classical type 2 diabetes (43,74–76), and in established type 2 diabetes, liver fat is supranormal (20). When ultrasound rather than magnetic resonance imaging is used, only more-severe degrees of steatosis are detected, and the prevalence of fatty liver is underestimated, with estimates of 70% of people with type 2 diabetes as having a fatty liver (76). Nonetheless, the prognostic power of merely the presence of a fatty liver is impressive of predicting the onset of type 2 diabetes. A large study of individuals with normal glucose tolerance at baseline showed a very low 8-year incidence of type 2 diabetes if fatty liver had been excluded at baseline, whereas if present, the hazard ratio for diabetes was 5.5 (range 3.6–8.5) (74). In support of this finding, a temporal progression from weight gain to raised liver enzyme levels and onward to hypertriglyceridemia and then glucose intolerance has been demonstrated (77).
They would often say to me, “Doctor. You’ve always said that weight loss is the key to reversing diabetes. Yet you prescribed me a drug that made me gain 25 pounds. How is that good?” I never had a good answer, because none existed. The truth was that insulin was not good for type 2 diabetes — it was only good for reducing blood glucose. The key was weight loss, whereupon the diabetes often goes away or at least gets significantly better. So, logically, insulin does not help reverse the disease, but actually worsens it.
The problem, of course, has not been solved – the sugar bowl is still overflowing. You’ve only moved sugar from the blood (where you could see it) into the body (where you couldn’t see it). So, the very next time you eat, the exact same thing happens. Sugar comes in, spills out into the blood and you take metformin to cram the sugar back into the body. This works for a while, but eventually, the body fills up with sugar, too. Now, that same dose of metformin cannot force any more sugar into the body.

Jump up ^ Qaseem A, Vijan S, Snow V, Cross JT, Weiss KB, Owens DK; Vijan; Snow; Cross; Weiss; Owens; Clinical Efficacy Assessment Subcommittee of the American College of Physicians (September 2007). "Glycemic control and type 2 diabetes mellitus: the optimal hemoglobin A1c targets. A guidance statement from the American College of Physicians". Annals of Internal Medicine. 147 (6): 417–22. doi:10.7326/0003-4819-147-6-200709180-00012. PMID 17876024. Retrieved 19 July 2008.


The food pyramid recommended 6-11 servings of carbs per day, and very little fat — a low-fat, high-carb diet. As we outlined in our last video, type 2 diabetes is a disease of carbohydrate intolerance. Someone with type 2 diabetes or prediabetes has a low carbohydrate tolerance, so eating carbs will lead to exaggerated blood sugar spikes. While those with a high carb tolerance may be able to eat a carb-heavy diet and remain healthy, someone with a low carb tolerance will experience chronic high blood sugar and likely even weight gain if they eat a high-carb diet.
Type 2 diabetes is usually first treated by increasing physical activity, and eliminating saturated fat and reducing sugar and carbohydrate intake with a goal of losing weight. These can restore insulin sensitivity even when the weight loss is modest, for example around 5 kg (10 to 15 lb), most especially when it is in abdominal fat deposits. Diets that are very low in saturated fats have been claimed to reverse insulin resistance.[79][80]
People with type 1 diabetes (T1D) can live long, happy lives with proper care and disease management. Advancements in medication types and delivery methods give people the freedom to choose which treatment options work best with their particular circumstance. T1D prognoses can be greatly improved with a combination of treatments and lifestyle choices.
Well, I don’t know much about VCRs, but I do know about type 2 diabetes. I can write an entire book about obesity (oh, wait, I did that already), or fasting (oh, wait, coming up) or type 2 diabetes (next up for 2018). But many of you will not want to go through the entire instruction manual. So this is the quick start guide for reversing your type 2 diabetes.

Levels which are significantly above or below this range are problematic and can in some cases be dangerous. A level of <3.8 mmol/L (<70 mg/dL) is usually described as a hypoglycemic attack (low blood sugar). Most diabetics know when they are going to "go hypo" and usually are able to eat some food or drink something sweet to raise levels. A patient who is hyperglycemic (high glucose) can also become temporarily hypoglycemic, under certain conditions (e.g. not eating regularly, or after strenuous exercise, followed by fatigue). Intensive efforts to achieve blood sugar levels close to normal have been shown to triple the risk of the most severe form of hypoglycemia, in which the patient requires assistance from by-standers in order to treat the episode.[8] In the United States, there were annually 48,500 hospitalizations for diabetic hypoglycemia and 13,100 for diabetic hypoglycemia resulting in coma in the period 1989 to 1991, before intensive blood sugar control was as widely recommended as today.[9] One study found that hospital admissions for diabetic hypoglycemia increased by 50% from 1990–1993 to 1997–2000, as strict blood sugar control efforts became more common.[10] Among intensively controlled type 1 diabetics, 55% of episodes of severe hypoglycemia occur during sleep, and 6% of all deaths in diabetics under the age of 40 are from nocturnal hypoglycemia in the so-called 'dead-in-bed syndrome,' while National Institute of Health statistics show that 2% to 4% of all deaths in diabetics are from hypoglycemia.[11] In children and adolescents following intensive blood sugar control, 21% of hypoglycemic episodes occurred without explanation.[12] In addition to the deaths caused by diabetic hypoglycemia, periods of severe low blood sugar can also cause permanent brain damage.[13] Although diabetic nerve disease is usually associated with hyperglycemia, hypoglycemia as well can initiate or worsen neuropathy in diabetics intensively struggling to reduce their hyperglycemia.[14]
Data from the Swedish randomized study of gastric banding showed that a loss of 20% body weight was associated with long-term remission in 73% of a bariatric surgery group, with weight change itself being the principal determinant of glucose control (13). Dietary weight loss of 15 kg allowed for reversal of diabetes in a small group of individuals recently receiving a diagnosis (21). In individuals strongly motivated to regain normal health, substantial weight loss is entirely possible by decreasing food consumption (88). This information should be made available to all people with type 2 diabetes, even though with present methods of changing eating habits, it is unlikely that weight loss can be achieved in those not strongly motivated to escape from diabetes. Some genetic predictors, especially the Ala12 allele at PPARG, of successful long-term weight loss have been identified (89), and use of such markers could guide future therapy. It must be noted that involuntary food shortage, such as a result of war, results in a sharp fall in type 2 diabetes prevalence (90,91).

The ripe fruit of this cactus has been shown in some small studies to lower blood sugar ­levels. You may be able to find the fruit in your grocery store, but if not, look for it as a juice or powder at health food stores. Researchers speculate that the fruit may possibly lower blood sugar because it contains components that work similarly to insulin. The fruit is also high in fiber. Try these foods for the best diabetic diet.
The study wasn’t a controlled experiment designed to prove whether or how treatment intensification might directly improve blood sugar. Researchers also lacked data to explain why doctors or patients might have decided against a change in therapy. And the study didn’t show whether failure to switch treatment regimens resulted in diabetes complications.
Dental care is therefore even more important for diabetic patients than for healthy individuals. Maintaining the teeth and gum healthy is done by taking some preventing measures such as regular appointments at a dentist and a very good oral hygiene. Also, oral health problems can be avoided by closely monitoring the blood sugar levels. Patients who keep better under control their blood sugar levels and diabetes are less likely to develop oral health problems when compared to diabetic patients who control their disease moderately or poorly.

In fact, the CDC notes that losing just 5 to 7 percent of your body weight can help lower your risk of developing type 2 diabetes. So, if you’re 200 pounds, aiming to lose about 10 to 14 pounds might help you prevent prediabetes from progressing to full-blown type 2 diabetes or help halt the advancement of type 2 diabetes if you’ve already been diagnosed.
Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic glucose production and, hence, on its sensitivity to suppression by insulin. Hepatic insulin sensitivity cannot be inferred from observed postprandial change in hepatic glycogen concentration because glucose transport into the hepatocyte is not rate limiting, unlike in muscle, and hyperglycemia itself drives the process of glycogen synthesis irrespective of insulin action. Indeed, postprandial glycogen storage in liver has been shown to be moderately impaired in type 2 diabetes (50) compared with the marked impairment in skeletal muscle (51).
Is this okay to use against gestational diabetes? I have PCOS and am pre-diabetic. I actually followed this way of eating (before seeing the Ted talk) with my first GD pregnancy and was scolded by the nutritionist. Yet my blood sugar was kept below 98 and I lost 15 lbs and our son’s blood sugar was perfect with an apgar of 10. So I’m thinking of just going this way again despite the ADA’s recommendations.
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Type 2 diabetes has long been known to progress despite glucose-lowering treatment, with 50% of individuals requiring insulin therapy within 10 years (1). This seemingly inexorable deterioration in control has been interpreted to mean that the condition is treatable but not curable. Clinical guidelines recognize this deterioration with algorithms of sequential addition of therapies. Insulin resistance and β-cell dysfunction are known to be the major pathophysiologic factors driving type 2 diabetes; however, these factors come into play with very different time courses. Insulin resistance in muscle is the earliest detectable abnormality of type 2 diabetes (2). In contrast, changes in insulin secretion determine both the onset of hyperglycemia and the progression toward insulin therapy (3,4). The etiology of each of these two major factors appears to be distinct. Insulin resistance may be caused by an insulin signaling defect (5), glucose transporter defect (6), or lipotoxicity (7), and β-cell dysfunction is postulated to be caused by amyloid deposition in the islets (8), oxidative stress (9), excess fatty acid (10), or lack of incretin effect (11). The demonstration of reversibility of type 2 diabetes offers the opportunity to evaluate the time sequence of pathophysiologic events during return to normal glucose metabolism and, hence, to unraveling the etiology.

There are several great exercises for diabetes, including biking, running, swimming, walking, strength training, and the like. The Centers for Disease Control and Prevention (CDC) recommends getting at least 150 minutes of moderate-intensity aerobic activity per week — that’s five 30-minute workouts — or 75 minutes of vigorous-intensity aerobic activity per week.
The new research ties in with recent thinking among experts about what happens when type 2 diabetes develops, says Domenico Accili, MD, chief of endocrinology at Columbia University Vagelos College of Physicians and Surgeons. "We have been talking for some time, that in diabetes, primarily type 2, the insulin-producing [beta] cell is not dead but simply inactive," he says. "If you put patients with diabetes on a diet, you can do marvels with their beta cells."
“People need to understand the continuum of diabetes,” she says. “If they’re on an upward trajectory of insulin resistance and a downward trajectory of insulin production weight loss, healthful eating and physical activity will slow down the insulin-loss trajectory and improve insulin sensitivity.” But, she says, “If they gain weight back, the diabetes comes back.”
Aside from the financial costs of diabetes, the more frightening findings are the complications and co-existing conditions. In 2014, 7.2 million hospital discharges were reported with diabetes as a listed diagnosis. Patients with diabetes were treated for major cardiovascular diseases, ischemic heart disease, stroke, lower-extremity amputation and diabetic ketoacidosis.
Any form of carbohydrate is eventually broken down by the body into glucose, a simple form of sugar. While the body can use glucose for fuel, levels that exceed what  is needed are toxic to the body. In the long run, that whole wheat muffin, cup of millet, or bowl of oatmeal turns into the exact same thing as a cup of soda, a donut or a handful of candy.
Although a close relationship exists among raised liver fat levels, insulin resistance, and raised liver enzyme levels (52), high levels of liver fat are not inevitably associated with hepatic insulin resistance. This is analogous to the discordance observed in the muscle of trained athletes in whom raised intramyocellular triacylglycerol is associated with high insulin sensitivity (53). This relationship is also seen in muscle of mice overexpressing the enzyme DGAT-1, which rapidly esterifies diacylglycerol to metabolically inert triacylglycerol (54). In both circumstances, raised intracellular triacylglycerol stores coexist with normal insulin sensitivity. When a variant of PNPLA3 was described as determining increased hepatic fat levels, it appeared that a major factor underlying nonalcoholic fatty liver disease and insulin resistance was identified (55). However, this relatively rare genetic variant is not associated with hepatic insulin resistance (56). Because the responsible G allele of PNPLA3 is believed to code for a lipase that is ineffective in triacylglycerol hydrolysis, it appears that diacylglycerol and fatty acids are sequestered as inert triacylglycerol, preventing any inhibitory effect on insulin signaling.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.

High blood sugar (hyperglycemia). Your blood sugar level can rise for many reasons, including eating too much, being sick or not taking enough glucose-lowering medication. Check your blood sugar level often, and watch for signs and symptoms of high blood sugar — frequent urination, increased thirst, dry mouth, blurred vision, fatigue and nausea. If you have hyperglycemia, you'll need to adjust your meal plan, medications or both.
Most doctors, dietitians and diabetes specialists claim that type 2 diabetes is a chronic and progressive disease. The American Diabetes Association, for example, almost proudly proclaims this on its website. Once you get the diagnosis, it’s a life sentence. But, it’s actually a great big lie. Type 2 diabetes is almost always reversible and this is almost ridiculously easy to prove. This is great news for the more than 50% of American adults who have been diagnosed with pre-diabetes or diabetes. Recognizing this truth is the crucial first step in reversing your diabetes or pre-diabetes. Actually, it something that most people already instinctively recognized to be true.
In a person with carbohydrate intolerance, type 2 diabetes or prediabetes, this system breaks down. The body loses its insulin sensitivity and more and more insulin is required to remove the excess blood sugar. As a result, blood sugar levels remain high and insulin levels are high as well, and these high insulin levels can make your body even less sensitive to insulin.
The first hint that type 2 diabetes is a fully reversible syndrome came from bariatric surgery. Almost a quarter century ago, Pories et al. (12) demonstrated that blood glucose levels normalized in obese people with type 2 diabetes undergoing bariatric surgery and that 10 years later, almost 90% remained free of diabetes. The phenomenon was more recently tested in a randomized prospective study comparing gastric banding with intensive medical therapy for type 2 diabetes (13). This least invasive type of surgery was most suitable for the randomized study, although it was associated with lower rates of diabetes reversal than other procedures. Mean fasting plasma glucose fell to normal levels in the surgically treated group but declined only modestly in the intensive medical treatment group despite oral agents and insulin (Fig. 1) (13). Remission of diabetes was related to the degree of weight loss rather than to group allocation and was achieved in 73% of the surgical group and 13% of the intensive medical treatment group because surgery was more effective in achieving weight loss as previously described (14). Type 2 diabetes can be reversed by applying a surgical procedure that diminishes fat mass.
But is John “free of diabetes”? This is where the lines become blurred. Medically speaking, the term “cure” is usually associated with acute disease—a temporary medical condition, such as bacterial pneumonia, that can be cured with antibiotics. For diabetes, which is a chronic disease, it may be more accurate to use the term “remission” rather than cure. Particularly when considering the pathology associated with diabetes and the individual’s genetic predisposition, relapse is always possible. In a consensus statement issued by the ADA, the term remission is defined based on the following definitions:2
The prevalence of prediabetes is also on the rise, as it’s estimated that almost 34 million U.S. adults were prediabetic in 2015. People with prediabetes have blood glucose levels that are above normal but below the defined threshold of diabetes. Without proper intervention, people with prediabetes are very likely to become type 2 diabetics within a decade.
As diabetes is a prime risk factor for cardiovascular disease, controlling other risk factors which may give rise to secondary conditions, as well as the diabetes itself, is one of the facets of diabetes management. Checking cholesterol, LDL, HDL and triglyceride levels may indicate hyperlipoproteinemia, which may warrant treatment with hypolipidemic drugs. Checking the blood pressure and keeping it within strict limits (using diet and antihypertensive treatment) protects against the retinal, renal and cardiovascular complications of diabetes. Regular follow-up by a podiatrist or other foot health specialists is encouraged to prevent the development of diabetic foot. Annual eye exams are suggested to monitor for progression of diabetic retinopathy.

Dr. Sarah Hallberg is a Medical Director at Virta Health. She also created the Medically Supervised Weight Loss Program at Indiana University Health Arnett and serves as its Medical Director. She is an adjunct Clinical Professor of Medicine at Indiana University School of Medicine. Dr. Hallberg is an expert in diabetes care and is board certified in Internal Medicine, Obesity Medicine, and Clinical Lipidology and also a Registered Clinical Exercise Physiologist from the ACSM.
Because many patients with diabetes have two or more comorbidities, they often require multiple medications. The prevalence of medication nonadherence is high among patients with chronic conditions, such as diabetes, and nonadherence is associated with public health issues and higher health care costs. One reason for nonadherence is the cost of medications. Being able to detect cost-related nonadherence is important for health care professionals, because this can lead to strategies to assist patients with problems paying for their medications. Some of these strategies are use of generic drugs or therapeutic alternatives, substituting a prescription drug with an over-the-counter medication, and pill-splitting. Interventions to improve adherence can achieve reductions in diabetes morbidity and mortality, as well as significant cost savings to the health care system.[62] Smartphone apps have been found to improve self-management and health outcomes in people with diabetes through functions such as specific reminder alarms,[63] while working with mental health professionals has also been found to help people with diabetes develop the skills to manage their medications and challenges of self-management effectively.[64]

An injection port has a short tube that you insert into the tissue beneath your skin. On the skin’s surface, an adhesive patch or dressing holds the port in place. You inject insulin through the port with a needle and syringe or an insulin pen. The port stays in place for a few days, and then you replace the port. With an injection port, you no longer puncture your skin for each shot—only when you apply a new port.
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